The long-term goal of this application to establish the mechanisms and circuitry by which signals from the upper respiratory tract integrate within the brainstem to produce reflex autonomic responses. Stimulation of the upper respiratory tract can produce an intense functional reorganization of the cardiovascular and respiratory systems. This reflex includes central apnea, parasympathetic bradycardia and sympathetically mediated vasoconstriction. Initiation of this response results from stimulation of trigeminal receptors that innervate the face and nasal passages. This autonomic response is primarily a defensive reflex, and is only elicited when a potentially life threatening external stimulus is presented. Because an animal is in imminent danger during such an event, homeostatic control, such as the maintenance or arterial blood pressure, should no longer be primary objective of the animal?s autonomic nervous system. In this situation a defensive reflex should temporarily become more powerful than a homeostatic reflex. It is hypothesized that stimulation of the trigeminal inhibits the baroreflex at the level of the nucleus tractus solitarius (NTS). The objectives of this proposal are to determine 1) the response of brainstem trigeminal neurons during nasal stimulation; 2) the relationship between the trigeminal system and secondary brainstem neurons located in the NTS and rostral ventrolateral medulla (RVLM); and 3) if trigeminal stimulation inhibits second-order barosensitive NTS neurons. It is expected that extracellular recordings will determine that neurons located within the superficial laminae of the trigeminal medullary dorsal horn (MDH) respond to nasal stimulation with an increase in firing rate that positively correlates with the cardiorespiratory changes elicited by the nasal stimulation. It is also expected that electrical stimulation of the NTS and RVLM will antidromically stimulate these same MDH neurons. This would determine that these nuclei are part of the brainstem circuitry of this response. Finally, it is expected that extracellular recordings will determine that trigeminal stimulation inhibits barosensitive neurons within the NTS, thus inhibiting the brainstem baroreflex pathway. This would indicate that a defensive reflex (upper respiratory tract stimulation) can inhibit a homeostatic reflex (arterial baroreflex). This proposal has clinical implications because it investigates the relationship between a defensive reflex and a homeostatic reflex, and explores the mechanisms of integrative cardiorespiratory control within the brainstem. Also, stimulation of the upper respiratory tract may be a casual factor in Sudden Infant Death Syndrome (SIDS). Some infants at risk for SIDS present autonomic dysfunction and abnormalities of respiratory and/or cardiovascular control mechanisms, especially after stimulation of the upper respiratory tract. Having a better understanding of brainstem cardiorespiratory integration might provide a neurological basis for the etiology of SIDS.